<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Lechtreck, Karl-Ferdinand</style></author><author><style face="normal" font="default" size="100%">Delmotte, P.</style></author><author><style face="normal" font="default" size="100%">Robinson, M. L.</style></author><author><style face="normal" font="default" size="100%">Sanderson, M. J.</style></author><author><style face="normal" font="default" size="100%">Witman, G. B.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Mutations in Hydin impair ciliary motility in mice</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of Cell Biology</style></secondary-title><short-title><style face="normal" font="default" size="100%">J Cell Biol</style></short-title></titles><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">02/2008</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2234243/</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">180</style></volume><pages><style face="normal" font="default" size="100%">633 - 643</style></pages><isbn><style face="normal" font="default" size="100%">0021-95251540-8140</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Chlamydomonas reinhardtii hydin is a central pair protein required for flagellar motility, and mice with Hydin defects develop lethal hydrocephalus. To determine if defects in Hydin cause hydrocephalus through a mechanism involving cilia, we compared the morphology, ultrastructure, and activity of cilia in wild-type and hydin mutant mice strains. The length and density of cilia in the brains of mutant animals is normal. The ciliary axoneme is normal with respect to the 9 + 2 microtubules, dynein arms, and radial spokes but one of the two central microtubules lacks a specific projection. The hydin mutant cilia are unable to bend normally, ciliary beat frequency is reduced, and the cilia tend to stall. As a result, these cilia are incapable of generating fluid flow. Similar defects are observed for cilia in trachea. We conclude that hydrocephalus in hydin mutants is caused by a central pair defect impairing ciliary motility and fluid transport in the brain.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">&lt;p&gt;200710162[PII]18250199[pmid]18250199[pmid]&lt;/p&gt;
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